Gastritis, gastric ulcer and duodenal ulcer are diseases which develop as a result of complicated entanglement of factors such as stress, genetic predisposition and lifestyle habit. In recent years, attention is being paid to the bacterium Helicobacter pylori (H. pylori) as one of the principal causes. Since the success of Warren and Marshall in the isolation and culture of spiral-shaped bacteria from gastric biopsy specimens in 1983, vigorous research has been carried out on the relationship between the subject bacteria and gastritis, gastric ulcer, duodenal ulcer and gastric cancer. As a result, the infection rate of Helicobacter pylori (H. pylori) is reported to be such that while the positive rate in normal stomach was about 4%, the positive rate was as high as about 83% for chronic gastritis, about 69% for gastric ulcer, about 92% for duodenal ulcer, and about 51% for non-ulcer dyspepsia syndrome (see Non-Patent Document 1). Furthermore, infection by the bacterium Helicobacter pylori is strongly correlated to the incidence rate of gastric cancer, and in 1994, the International Agency for Research on Cancer of the WHO declared the bacterium Helicobacter pylori as a carcinogen indicating a strong causal relationship.
The mainstream of the treatment for gastritis, gastric ulcer, duodenal ulcer and the like has been represented by symptomatic therapy, in which gastric acid secretion inhibitors which inhibit gastric acid secretion, such as H2 blockers and proton pump inhibitors, and mucosal protective agents are utilized for the purpose of improving subjective symptoms such as epigastric pain, and accelerating the healing of gastric ulcer. However, it is reported that even though the lesions are temporarily healed by these drugs, if the treatment is stopped, about 80% of the patients have a relapse within one year (see Non-Patent Document 1). On the other hand, it is also reported that when Helicobacter pylori bacteria are eradicated, the one-year recurrence rate was 10% or less for duodenal ulcer, and the rate was low also for the case of gastric ulcer (see Non-Patent Document 2).
Currently, as a method for eradicating Helicobacter pylori bacteria, treatment is carried out, such as by using a proton pump inhibitor (PPI) in combination with antibacterial agents such as amoxicillin and clarithromycin, in large quantities over one week or more, and in some cases, adding metronidazole thereto. However, administration of antibacterial agents in large quantities also causes disinfection of useful bacteria in the intestine, and as a result, there is concern for adverse side effects such as loose stool, diarrhea and taste disturbance, glossitis, stomatitis, abnormality of hepatic function, and hemorrhagic enteritis, as well as the possibility of promoting the emergence of methicillin-resistant Staphylococcus aureus (MRSA).
To date, a large number of patent applications have been filed with regard to pyridine derivatives, for the applications as antiulcer agents, gastric acid secretion inhibitors, antibacterial agents against Helicobacter pylori bacteria, and the like (see Patent Documents 1 to 8). However, there is not found any compound which combines an anti-Helicobacter pylori action and a gastric acid secretion inhibiting action in a well balanced manner, and is capable of eradicating Helicobacter pylori bacteria, when used as a sole agent.
Furthermore, a compound having an anti-Helicobacter pylori action in vitro and a gastric acid secretion inhibiting action has been discovered (see Non-Patent Document 3). However, in a Helicobacter pylori-infected model using Mongolian gerbil, which is considered to reflect human infection by Helicobacter pylori bacteria, the effectiveness could not be verified, and development of the agent has been abandoned.
In spite of such extensive efforts as described above, triple therapy is still widely practiced at present, for the eradication of Helicobacter pylori bacteria. The reason is that proton pump inhibitors such as omeprazole, lansoprazole and rabeprazole, and clarithromycin are all extremely unstable in acid, and it is difficult with amoxicillin to exhibit antibacterial activity under acidic conditions. That is, there was a need to administer large quantities of the aforementioned acid-labile antibiotic substances, while gastric acid had been strongly inhibited by proton pump inhibitors which were administered as an enteric preparation.    Patent Document 1: JP-A No. 61-50979    Patent Document 2: JP-A No. 3-173817    Patent Document 3: JP-A No. 5-247035    Patent Document 4: JP-A No. 59-181277    Patent Document 5: JP-A No. 7-69888    Patent Document 6: JP-A No. 3-48680    Patent Document 7: JP-A No. 2-209809    Patent Document 8: JP-A No. 58-39622    Non-Patent Document 1: Martin J. Blaser: Clin. Infectious Disease, 15; 386-393, 1992    Non-Patent Document 2: Graham D. Y., et al.: Ann. Intern. Med., 116; 705-708, 1992    Non-Patent Document 3: Thomas C. Kuehler, et al., J. Med. Chem. 1998, 41, 1777-1788